Protein kinase networks that limit TLR signalling. (23rd January 2014)

• Record Type: Journal Article
• Authors: Clark, Kristopher
• Is Part Of: Biochemical Society transactions. Volume 42:Number 1(2014)
• Page Start: 11
• Page End: 24
• Publication Date: 2014-01-23
• Subjects: inhibitor of nuclear factor κB kinase (IKK) -- innate immunity -- mitogen-activated protein kinase (MAPK) -- phosphoinositide 3-kinase (PI3K) -- salt-inducible kinase (SIK) -- Toll-like receptor (TLR); Biochemistry -- Congresses; 572
• DOI: 10.1042/BST20130124
• Languages: English
• ISSNs: 0300-5127

Abstract

Abstract : TLRs (Toll-like receptors) detect invading micro-organisms which triggers the production of pro-inflammatory mediators needed to combat infection. Although these signalling networks are required to protect the host against invading pathogens, dysregulation of TLR pathways contributes to the development of chronic inflammatory diseases and autoimmune disorders. Molecular mechanisms have therefore evolved to restrict the strength of TLR signalling. In the present review, I highlight recent advances in our understanding of the protein kinase networks required to suppress the innate immune response by negatively regulating TLR signalling and/or promoting the secretion of anti-inflammatory cytokines. I present my discoveries on the key roles of the IKK (inhibitor of nuclear factor κB kinase)-related kinases and the SIKs (salt-inducible kinases) in limiting innate immunity within the greater context of the field.